Objective: The current study aimed to assess the viability of sympathetic sudomotor fibers in patients suffering from mild peripheral arterial occlusive disease (PAD). Methods: Sympathetic skin response (SSR) from the hand (electrical stimulation) and sole (electrical and magnetic stimulation) of 25 patients with PAD (19 males and 6 females with mean age 62.7±10.2 years) was recorded unilaterally depending on the side of the affected limb (18 right side, 7 left side). Electrophysiological data were also collected and correlated with the SSR results. Twenty-five, age-and gender-matched healthy volunteers served as controls. Results: No evidence of nerve conduction abnormalities was recorded from the group of patients. Intact SSR recordings were obtained from the upper limb of patients. Nine patients (36%) had absent SSR in the lower limb following electrical stimulation, whilst the same 9 patients had absent SSR following magnetic stimulation. Significant differences occurred between groups in the SSR latency scores recorded from the lower limb. Following electrical stimulation the mean SSR latency in patients was significantly prolonged, compared to that of controls (P=0.000), whilst the same applied following magnetic stimulation (P=0.000). There was no correlation between SSR abnormalities and nerve conduction measurements. The manifestation of intermittent claudication at a walking distance of 250 m was strongly correlated w ith absent lower limb SSR (r=0.71, P=0.035). Conclusions: SSR abnormalities appe ared to be an early and independent finding of neural impairment in our patients . Significance: SSR study, performed at an early stage of PAD may prove useful i n differentiating PAD-induced neuropathy from other neuropathic processes. Objective: The current study aimed to assess the viability of sympathetic sudomotor fibers in patients suffering from mild peripheral arterial occlusive disease (PAD). Methods: Sympathetic skin response (SSR) from the hand (electrical stimulation) and sole (electrical and magnetic stimulation) of 25 patients with PAD (19 males and 6 females with mean age 62.7 ± 10.2 years) was recorded unilaterally depending on the side of the affected limb (18 right side, 7 left side). Electrophysiological data were also collected and correlated with the SSR Results: No evidence of nerve conduction abnormalities was recorded from the group of patients. Intact SSR recordings were obtained from the upper limb of patients. Nine patients (36 %) had absent SSR in the lower limb following electrical stimulation, whilst the same 9 patients had absent SSR following magnetic stimulation. Significant differences occurred between g roups in the SSR latency scores were recorded from the lower limb. Following electrical stimulation the mean SSR latency in patients was significantly prolonged, compared to that of controls (P = 0.000), whilst the same applied following magnetic stimulation (P = 0.000). There was no correlation between SSR abnormalities and nerve conduction measurements. The manifestation of intermittent claudication at a walking distance of 250 m was strong correlated w ith absent lower limb SSR (r = 0.71, P = 0.035). Conclusions: SSR abnormalities appe ared to be an early and independent finding of neural impairment in our patients. Significance: SSR study, performed at an early stage of PAD may prove useful in differentiating PAD-induced neuropathy from other neuropathic processes.